[Persistent activation and/or reactivation in the subacute phase of unstable angina. Reasons for prolonged antithrombotic treatment].

Coronary artery thrombosis, due to a rupture of the vulnerable plaque, plays an important role in acute coronary syndromes. The interaction between platelets and thrombin with ruptured vulnerable plaque trigger a complex mechanism. The clinical manifestations depend on the extent and duration of thrombus formation. In the acute phase, aspirin, heparin and the new drugs reduce ischemic clinical outcomes. However, clinical rebound after withdrawal antithrombotic therapy has been observed and, follow-up studies have also documented a high risk of recurrence in the following months. A hypercoagulable state, thrombin generation and activation and haematological rebound is shown in acute coronary syndrome patients. Thus, the goal of treatment could be to control thrombotic response in the acute phase and to allow the healing and stabilization of the culprit lesion to avoid clinical ischemic events in the long-term.